Collective ERK/Akt activity waves orchestrate epithelial homeostasis by driving apoptosis-induced survival

Gagliardi, Paolo Armando; Dobrzyński, Maciej; Jacques, Marc‐Antoine; Dessauges, Coralie; Ender, Pascal; Blum, Yannick; Hughes, Robert M.; Cohen, Andrew R.; Pertz, Olivier

doi:10.1016/j.devcel.2021.05.007

Cited by 109 publications

(108 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Another key question is how biochemical signaling, including mitogenic signaling, that emerges from the apoptotic process, contributes to compensatory proliferation. It has been shown recently that extracellular-signal-regulated kinase (ERK) is activated in most of the neighboring cells upon apoptosis and acts as a survival factor for these cells [32,33]. Our data support the idea that mitogenic signals secreted from the apoptotic cell are crucial as demonstrated before [5–11], but not solely sufficient, to explain the spatially inhomogeneous nature of compensatory proliferation.…”

Section: Discussionsupporting

confidence: 89%

Mechanics defines the spatial pattern of compensatory proliferation

Kawaue

Yow

et al. 2021

Preprint

View full text Add to dashboard Cite

The number of cells in tissues is tightly controlled by cell division and cell death, and misregulation of cell numbers could lead to pathological conditions such as cancer. To maintain cell numbers in a tissue, a cell elimination process named programmed cell death or apoptosis, stimulates the proliferation of neighboring cells. This mechanism is called apoptosis-induced compensatory proliferation, which was originally reported more than 40 years ago. While only a limited number of the neigboring cells need to divide to compensate for apoptotic cell loss, the mechanisms that select cells for undergoing division remain an open question. Here we found that the spatial inhomogeneity in mechanotransduction through a growth-promoting transcription co-activator Yes-associated protein (YAP) in the neighboring tissue, accounts for the inhomogeneity of compensatory proliferation. Such inhomogeneous mechanotransduction arises from the combination of the non-uniform distribution of nuclear size, which is inherent in tissues, and the non-uniform pattern of mechanical force applied to the neighboring cells upon apoptosis. Our findings from a mechanical perspective complement the current biochemical understanding of compensatory growth and provide additional insights into cellular functions of how tissue precisely maintains its homeostasis.

show abstract

Section: Discussionsupporting

confidence: 89%

Mechanics defines the spatial pattern of compensatory proliferation

Kawaue

Yow

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Beyond elucidating cell fates represented in the WE or the AEC tissues, the behavioral properties of such populations and the molecular mechanisms enabling their formation on the amputation plane remain largely unknown. For example, mechanical damage has been implicated in creating Erk activation that temporarily spreads from the damaged region to the surrounding area, forming wave patterns, influencing epithelial cell migration and survival ( Aoki et al, 2017 ; Hino et al, 2020 ; Gagliardi et al, 2021 ). Yet the implication of such Erk activity spreading for wound closure and limb regeneration remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Tissues and Cell Types of Appendage Regeneration: A Detailed Look at the Wound Epidermis and Its Specialized Forms

Aztekin

2021

Front. Physiol.

View full text Add to dashboard Cite

Therapeutic implementation of human limb regeneration is a daring aim. Studying species that can regrow their lost appendages provides clues on how such a feat can be achieved in mammals. One of the unique features of regeneration-competent species lies in their ability to seal the amputation plane with a scar-free wound epithelium. Subsequently, this wound epithelium advances and becomes a specialized wound epidermis (WE) which is hypothesized to be the essential component of regenerative success. Recently, the WE and specialized WE terminologies have been used interchangeably. However, these tissues were historically separated, and contemporary limb regeneration studies have provided critical new information which allows us to distinguish them. Here, I will summarize tissue-level observations and recently identified cell types of WE and their specialized forms in different regeneration models.

show abstract

“…Quantitative imaging approaches have revealed that the epithelial cells tend to be eliminated by compression-driven ERK inactivation (Moreno et al, 2019), and the extruding cells are governed through an interplay between actomyosin contractility and cell junctions (Lubkov and Bar-Sagi, 2014;Thomas et al, 2020). Moreover, the neighboring cell behaviors are also physically affected by the extruding cells through intercellular signal transmissions, such as calcium and ERK activation waves (Takeuchi et al, 2020;Gagliardi et al, 2021;Valon et al, 2021). These findings led to accelerating studies on mechanical cell competitionthe mechanism for eliminating unfit cells for the tissue homeostasis (Brás-Pereira and Moreno, 2018;Matamoro-Vidal and Levayer, 2019).…”

Section: Maintenance Of Epithelial Tissue Volume By Controlling Cell ...mentioning

confidence: 99%

Mechanical Feedback Control for Multicellular Tissue Size Maintenance: A Minireview

Hirashima

2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

All living tissues and organs have their respective sizes, critical to various biological functions, such as development, growth, and homeostasis. As tissues and organs generally converge to a certain size, intrinsic regulatory mechanisms may be involved in the maintenance of size regulation. In recent years, important findings regarding size regulation have been obtained from diverse disciplines at the molecular and cellular levels. Here, I briefly review the size regulation of biological tissues from the perspective of control systems. This minireview focuses on how feedback systems engage in tissue size maintenance through the mechanical interactions of constituent cell collectives through intracellular signaling. I introduce a general framework of a feedback control system for tissue size regulation, followed by two examples: maintenance of epithelial tissue volume and epithelial tube diameter. The examples deliver the idea of how cellular mechano-response works for maintaining tissue size.

show abstract

Collective ERK/Akt activity waves orchestrate epithelial homeostasis by driving apoptosis-induced survival

Cited by 109 publications

References 61 publications

Mechanics defines the spatial pattern of compensatory proliferation

Mechanics defines the spatial pattern of compensatory proliferation

Tissues and Cell Types of Appendage Regeneration: A Detailed Look at the Wound Epidermis and Its Specialized Forms

Mechanical Feedback Control for Multicellular Tissue Size Maintenance: A Minireview

Contact Info

Product

Resources

About